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Flashcards in GI disorders Deck (101):

Cirrhosis - Later Clinical Manifestations 


Cirrhosis - most common causes 

1. Alcoholism 

2. Hepatitis B & C

3. Hepatotoxic meds 


Cirrhosis - patho 

Infiltration + accumulation of fatty deposits - fibrotic changes - destroy hepatocytes = widespread scar formation - decreased liver function - obstructed blood flow - increased portal pressure 


Cirrhosis - S/s early 


Generalized fatigue 

Abdominal pain 

GI symptoms - N+V, diarrhea 


Cirrhosis - S/s - disease progression 

Weight loss




Esophageal varices 

Portal HTN

Telengiectasis (spider angiomas) 


Cirrhosis - Jaundice (Icterus) - causes & S/s 

Obstructed billary ducts

Liver cannot breakdown old RBCs 

1. Steatorrhea - white, clay color stool - bile needed to break down fat 

2. Dark urine (maple syrup) - kidneys filter elevated billirubin from blood 

3. Pruritus 


Cirrhosis - Ascites - patho 

increased hydrostatic pressure from portal HTN → blood proteins leak into peritoneum; liver unable to synthesize protein → low blood albumin; fluid shifts out of vascular
system into peritoneum → third-spacing occurs; liver cannot metabolize aldosterone → kidneys
retain Na & water; increased vascular volume → further leakage of fluid into abdominal cavity


Cirrhosis - Ascites - S/s 

Weight gain 

Abdominal (umbilical) hernias 

Abdominal distention 


Cirrhosis - Ascites - TX

1. Low sodium diet 

2. Aldosterone antagonist - Spironolactone (Aldactone) 

3. Paracentesis - symptomatic relief - sitting up or side lying ; suprapubic - empty bladder ; Monitor - VS, weight (pre and post), I+O, electrolytes 

4. Refractory ascites - TIPS - catheter and shunt within hepatic system - connects to the jugular 


Cirrhosis - Portal HTN - patho 

increased pressure from fibrotic changes → back-up of blood in GIsystem → splenomegaly; veins in esophagus, stomach, intestines, abdominal wall & rectum
dilate → esophageal varices, prominent abdominal veins, hemorrhoids, ascites. 


Cirrhosis - Esophageal varices 

Patho - thinner, less elastic esophageal veins unable to compensate for increasedpressure → pressure increases, varices enlarge, begin to bleed
1. Frank hematemesis - vomitting blood 
2. Coffee-ground emesis
3. Melena, (black tarry stools)


Cirrhosis - Esophageal varices and portal HTN - TX

1. Reduce portal HTN - beta-blockers + nitrates 

2. EGD + banding or ligation 

3. EGD + Sclerotherapy 

4. Acute !!! - vasoconstrictive meds - IV - Vasopressin or octreotide 

5. Sengstaken-Blakemore or Minnesota tube - Airway !!!- pt intubated, on the vent, sedated 


Esophageal varices - IV Vasopressin vs IV Octreotide 

1. IV Vasopressin - systemic - can worsen portal HTN 

2. IV Octreotide (Sandostatin) - specific - constricts just GI area 


Cirrhosis - Hepatic Encephalopathy - patho 

Elevated ammonia & toxins in blood
1. Ammonia - by-product of digestion of dietary & blood proteins
2. Ammonia absorbed from intestinal tract not metabolized by diseased liver
3. Ammonia accumulates in blood
a. Altered mental states: Confusion → coma
b. Asterixis - flapping tremor of hands
4. High protein diet & GI bleeding - aggravate condition (more protein) 


Cirrhosis - Hepatic Encephalopathy - TX

1. Lactulose 

2. Low protein diet ; early in cirrhois - high protein 

3. Neomycin - antibiotic - decrease bacterial flora needed to breakdown protein 



Promote excretion of ammonia ; tx of constipation 

Improvement in mental status 

Expect 2-3 soft stools/day 

Watch for diarrhea 

Coma - NG, rectal 


Cirrhosis DX

1. LABS: Liver function panel, serum ammonia, clotting studies, protein + albumin, bilirubin , CBC, H+H, vitamin deficiencies

2. CT, MRI, US

3. Liver biopsy - Definitive !!! - supine, arm elevated behind head , US guided, between ribs - BLEEDING - stay for 6 hrs, H+H compared 


Liver Functions 

  1.  Metabolism :Glucose, fat, proteins 
  2. Conversion: Ammonia to urea
  3. Detoxification: Drugs, alcohol, toxins
  4. Breakdown of RBCs: Formation of bile
  5. Production: Clotting factors, blood proteins, enzymes 


Hepatitis A (HAV) - causes  

Transmitted by the fecal-oral route
1. Non-life threatening, usually self-limiting 


HAV - Prevention 

1. Good hand washing
2. Avoid contaminated food & water
3. If exposed, receive IgG within 2 weeks
4. Get vaccinated (HAVRIX & VAQTA) if:
a. traveling to areas with high incidence
b. living in crowded conditions
c. working in correctional facilities, day-care centers, long-tem care


Hepatitis B (HBV) - causes 

Transmitted through blood & serum
1. Unprotected sex
2. Sharing needles or through accidental needle sticks
3. Blood transfusions before 1992
4. Hemodialysis
5. Maternal-fetal route
6. Cosmetic procedure like tattooing & body piercing


HBV - Prevention 

1. Avoid exposure to blood & body fluids
2. Follow standard precaution
3. Use needless systems
4. Get Vaccinated - 3 doses - 1st; 2nd 1 mo later; 3rd 2 mo after 2nd.  


Hepatitis C (HCV) - causes 

Transmitted blood to blood
1. Sharing needles - illicit drug users have highest incidence
2. Receiving blood products or organ transplant before 1992
3. Unsanitary tattoo or piercing equipment
4. Sharing tools for snorting cocaine 


HCV - Prevention and labs 

Education of high-risk groups 

1. Enzyme-linked immunosorbent assay (ELISA)
2. Recombinant immunoblot assay (RIBA)

Liver biopsy 


Chronic hepatitis - TX 

A. Rest - promote regeneration & healing, reduce metabolic demands on liver

B. Nutrition - high CHO, normal protein & fat content, small freq meals

C. Medications
1. Antiemetics
2. Antiviral drugs - reduce the viral load
Antiretroviral agents
3. Immunomodulator


Chronic hepatitis - Education 

1. Prevent spread of infection

2. Avoid alcohol and OTC mediations (acetaminophen)

3. If traveling - drink bottle water, or water from purification system, avoid foods washed or prepared with tap water (fresh fruits & vegetables)

* Complications - cirrhosis & liver cancer


Hepatitis - causes 

Viral (most common), hepatotoxic medications, alcohol, altered immune
responses environmental toxins


Hepatitis - patho 

- liver becomes enlarged & congested with
inflammatory cells, lymphocytes & fluid; widespread inflammation & edema leads to
increased pressure within liver portal system, interferes with blood flow → ischemia &
necrosis; edema of the biliary ducts → obstruction & jaundice 


Primary liver cancer
- two types

1. Hepatocellular carcinoma - develops from hepatocytes
a. 90% linked to chronic viral hepatitis, & cirrhosis.
2. Cholangiocarcinoma - originates from bile duct cells

Liver Biopsy - definitive diagnosis

Treatment - palliative
1. Surgery
2. Chemotherapy and hepatic artery embolization

3. Liver transplant


Pancreatitis - patho 

Autodigestion of pancreatic tissue by pancreatic enzymes
a. Obstruction of the pancreatic duct → increased production of pancreatic enzymes (lipase, trypsin, kallikrein). Activation of enzymes → vasodilation,
increased vascular permeability, edema, necrosis & hemorrhage 


Pancreatitis - causes 

1. Cholelithiasis
2. Alcohol & drug use
3. Pancreatic tumors or cysts
4. Abdominal trauma, surgical manipulation
5. Infection 

6. Corticosteroids, Thiazide diuretics (Hydrochlorothiazide)


Pancreatitis - Pain 

Severe pain
a. Midepigastric or LUQ pain - can radiate to the back or left shoulder
b. N & V
c. Assume fetal position


Pancreatitis - Pain TX

1. NPO – bowel rest; possible NG tube

2. IV hydration

3.  Analgesics – Dilaudid, Morphine, Fentanyl, Dilaudid 

4.  Anticholinergics - Bentyl, Pro-Banthine

5. Antisecretory agents - somatostatin & octreotide

6. Antiemetic

7.PPIs & H2 blockers 

8. Antispasmodic (Vistaril, Atarax) 



Bentyl & Pro-Banthine 

Anticholinergic - decrease GI motility - decrease secretion of pancreatic enzymes 

TX of pancreatic pain 

SE - dry mouth 


1. Serum amylase

2. Serum lipase 

1. elevated 1st 

2. more DX - elevated for longer 

* Classic labs for pancreatitis 

In addition - Hypocalcemia - Tetany (Chvostek’s and Trousseau’s sign).


Pancreatitis - Complications 

1. Hypovolemia, hemorrhage & shock

2.  Acute renal failure

3.  Respiratory complications - pleural effusion, atelectasis, & pneumonia, leading to ARDS

4. DIC

5. Diabetes mellitus

6. Sepsis & Multi-organ system failure (MOSF)


Pancreatitis - Diet 

1. Small frequent meals - 4-6 times/day

2. Low fat, high carbs and protein 

3. Bland food - no spices or stimulants 


Pancreas - function 

1.Exocrine gland enzymes - help break down carbohydrates, fats, proteins, and acids in the duodenum. These enzymes travel down the pancreatic duct into the bile duct in an inactive form. When they enter the duodenum, they are activated. The exocrine tissue also secretes a bicarbonate to neutralize stomach acid in the duodenum.
2.Endocrine gland hormones - insulin and glucagon (which regulate the level of glucose in the blood), and somatostatin (which prevents the release of the other two hormones).


1. Turner's sign 

2. Cullen's sign 

1. flank discoloration (ecchymosis) 

2. periumbilical ecchymosis 

** Necrotizing, hemorrhagic pancreatitis 


Cholecystitis vs Cholelithiasis

inflammation of the GB vs stones in the gallbladder


Bile function 

is the greenish-yellow fluid (consisting of waste products, cholesterol, and bile salts) that is secreted by the liver cells to perform two primary functions, including the following:

To carry away waste
To break down fats during digestion


Biliary system function 

bile ducts, gallbladder, and associated structures

To drain waste products from the liver into the duodenum
To help in digestion with the controlled release of bile


Stone formation & pathophysiology

a. abnormal metabolism of cholesterol & bile salts
b. Stones form → irritate the GB wall → inflammation. Stones block cystic duct → trapped bile causes chemical irritation of GB. Irritation → edema &
distention → interferes with circulation. Infection &  ischemia → necrosis &
gangrene. Severe edema → perforation & peritonitis 


GB disease - S/s 

1.GI distress - dyspepsia; bloating & flatulence; N & V
2. Pain - Biliary colic
3. Fever - Tachycardia
4.Jaundice - pruritus; dark urine; steatorrhea;
impaired absorption of fat soluble vitamins


GB disease - Somatostatin + Octreotide 

antisecretory agents, antiinflammatory properties - used to decrease risk of pancreatitis with Endoscopic retrograde cholangiopancreatography (ERCP)


Crohn's - common location + appearance 

Ileocecal area (RLQ) 

Patchy, cobblestone appearence, edematous 


Crohn's - S/s 

1. Diarrhea - 5-6 loose stools - non bloody 

2. Weight loss

3. Nutritional deficiencies - anemia, low albumin; steatorrhea 

4. Pain - RLQ 

5. Fever + leukocytosis 


Crohn's - complications 

Fistulas & abcesses - peritonitis/perforation 


Crohn's - DX

CBC, ESR + CRP. electrolytes, Imaging studies, albumin, folic acid, B12, iron 



Crohn's & Ulcerative colitis - TX

1. Aminosalicylates - 5 ASA

2. Steroids 

3. Immunomodulators 

4. Antidiarrheals

5. Anti-infective - tx fistulas + abcesses


Sulfasalazine (Azulfidine) 

Aminosalicylates - 5 ASA - inhibit prostaglandins - anti-inflammatory effect 

tx of Crohn's + Ulcerative Colitis 

Assess for sulfa allergies 

PO - full glass of water - to avoid crystallization of the urine 

Takes 2-4 weeks to work 


Balsalazide vs Mesalamine (Ascol) 

works in colon - tx of ulcerative colitis 


works in terminal ileum - tx of Crohn's 

* Fluids to avoid crystallization of the urine 

Aminosalicylates - 4 ASA 


Infliximab (Remicade) - IV 


Humira - subcut 

Immunomodulators - tx of Crohn's + Ulcerative Colitis 





Antidiarrheals - tx Crohn's 

Caution - Ulcerative colitis - Toxic megacolon !!! - dilation of the colon - perforation 


Ulcerative Colitis - common location + appearance 

Rectosigmoid colon (end of large intestine) - LLQ

Very red, edematous, continuous 


Ulcerative Colitis  - S/s 

1. Up to 20 diarrhea stools/day - bloody + mucus stools 

2. Weight loss

3. Pain LLQ

4. Tenesmus - urgent sensation to defecate 

5. Extraintestinal symptoms 


Oral lesions



Ulcerative Colitis - complications 



Sclerosing cholangitis - inflammation of the gallblader and ducts around it 

Increased risk for colon cancer 


Ulcerative Colitis - DX 


+ Liver panel and Colonoscopy /Bx 


Diverticula - common location and cause 

Herniations or out-pouching of the intestinal wall 

sigmoid colon 

Low fiber diet 

Evident in 50 % of people over 80 

DX: colonoscopy 


Diverticulosis vs Diverticulitis 

Presence of many herniations 


Inflammation of one or more deverticula 


Diverticula - TX

1. Bowel rest - NPO - progress to clear liquids, low fiber diet - teach about increasing fiber gradually - 25-30 grams 

2. Anti-infectives - Flagyl or Cipro 


Colon Cancer - Risk 

Family hx of polyps

Hx of ulcerative colitis

Age over 50, male

Diet - high fat, red meat, processed carbs, low fiber, fried + grilled foods. 


Familial adenomatous polyposis FAP



Colon Cancer - 55 % in rectosigmoid colon - S/s 

1. Rectal bleeding - Hematochezia - bright red blood 

2. Stool narrow, ribbon-like

3. Straining to defecate 


Colon Cancer - ascending colon - S/s 

1.Rectal bleeding -  black, tarry, mahogany color 

2. Anemia

3. Little change in stool appearance 


Colon Cancer - DX

A. Labs - CBC, FOBT, CEA ( carcino-embrionic antigen)

B. Imaging Studies - Barium enema, CT, MRI

C. Procedures - Colonoscopy & sigmoidoscopy - direct visualization of the colon 


FOBT - fecal occult blood test 

Hemoccult test 

Don't eat red meat or anything red 

Do not contaminate with tissue or urine 

No NSAIDs or Steroids - GI irritation 

No Vitamins 

* Do not stop medication - keep in mind 


Colonoscopy - pre-care & during procedure 

1) Informed consent
2) NPO for 8 hours, except for certain medications
3) Cleanse bowel
a. Oral Go-Lytely
b. Enemas until clear

4) Establish IV access

During procedure
1) Administer oxygen & sedation - Benzodiazepines - Versed, Valium, Fentanyl 
2) Monitor airway & VS 


Colonoscopy - post-care 

Monitor VS frequently, q 15-30 minutes
a. Assess sedation levels and assess for any complications
b. Assess for rectal bleeding
c. Assist out-of-bed (OOB) to assess stability

Pain - expected - intermittent gassy, crampy pain 

!!! Continuous pain - rigid abdomen - perforated colon ? 


The American Joint Committee on Cancer TNM staging system

1. T (tumor) - how far the primary tumor has grown into the wall of the intestine;
has it spread locally to nearby areas.
2. N (nodes) - extent of spread to nearby lymph nodes
3. M (metastasis) - indicates if cancer has metastasized to other organs 


Hemicolectomy with anastomosis - laparascopic - post-care

remove tumor - reconect healthy pieces together + remove lymph nodes 

1. Incision 

2. Bowel sounds - absent or hypoactive for 24-48 hrs - NPO until return (ice chips) 

3. NG - decompress the bowel - prevent N+V 

4. Colostomy - maybe 

5. Pain - epidural PCA - assess pain + insertion site ; should be able to ambulate - moniot RR + Vitals + level of sedation 

6. Antibiotics - 24 hrs 


Teaching on screening guidelines for colorectal cancer 

Colonoscopy every year

Start screening age 50 unless high risk - Repeat every 10 years 

Stop at age 75

Flexible Sigmoidoscopy can be done instead (at the doctor's office) 


TPN - best practices 

A. Check physician's order and compare order with TPN formula
1) A new order must be written every day

B. Keep the solution refrigerated until ready to use

C. Wash hands, use aseptic technique, attach proper tubing with the appropriate filter to
solution bag

D. Regulate flow on an IV infusion pump

E. Monitor for complications and response to therapy

F. Assess daily labs, monitor daily weights and I & O
1) Blood sugars q 6 h with insulin coverage

G. Replace TPN/Lipid solutions and tubing q24h
1) Label bag with start & stop times

H. If next bag is not available, discontinue current bag, hang 10% or 20% dextrose

I. Never increase IV rate to “catch-up” 


TPN - complications 

1) Solution related - fluid & electrolyte imbalances

a. Hyperosmolar solution can cause fluid shifts resulting in hyper or hypovolemia

b. Hyperglycemia can cause osmotic diuresis leading to dehydration & hypovolemia

c. Sodium, potassium & calcium imbalances can occur

2) Infections
a. Contaminated solutions and IV catheters
i. strict aseptic technique is required when handling and
administering TPN. 


GI - Age related changes 

A. Poor dentition or ill-fitting dentures
B. Diminished sense of taste
C. Atrophy of the gastric mucosa
Decreased production of hydrochloric acid
a. less absorption of iron and cobalamin (vitamin B12)

D. Reduced GI motility

E. Loss of sphincter tone

F. Change in the structure/function of the pancreatic duct

G. Decrease in liver cells 


Liver enzymes

1. Aspartate aminotransferase (AST)
2. Alanine aminotransferase (ALT)
3. Alkaline phosphatase (ALP)
4. Lactic dehydrogenase (LDH)


Esophagogastroduodenoscopy (EGD) - visualization of the esophagus, stomach &

a. Informed consent
b. NPO for 8 hours, except for certain medications
c. Establish IV access

 During procedure
a. Administer oxygen & sedation
b. Monitor airway & VS

a. Monitor VS frequently, q 15-30 minutes
Assess sedation levels and assess for any complications
b. Keep NPO until the gag reflex returns
Prevent aspiration of food or fluids
c. Assist out-of-bed (OOB) to assess stability


Endoscopic retrograde cholangiopancreatography (ERCP)

EGD with visualization of the biliary and pancreatic ducts using radio opaque dye

Pre & post care - similar to EGD

Additional complications specific to an ERCP

a. gallbladder inflammation & pancreatitis


Liver bipsy - pre-care + post-care 

1) Informed consent needed
2) NPO 8 hours
3) Obtain coagulation studies, type & cross match, and baseline CBC
4) Instruct pt on the procedure

1) Assess VS frequently: q 15 min. x 2, then q 30 min. x4, then q 1 hour x 4.
2) Position
a. right side for 2 hours to splint puncture site, then flat for up to 12 hours
3) Assess puncture site 



weakness in a muscle wall that allows the partial or complete protrusion of an organ through the weakened area 

Signs & symptoms
A. Lump or protrusion
B. Strangulated hernia
1. Abdominal distention, N & V, pain, fever, and tachycardia - tx : resection of the ischemic bowel with temporary colonoscopy  

Urinary complications - void within 6-8 hrs 


Complications of
intestinal obstructions 

acid-base and electrolyte imbalances

Fluid, gas & intestinal contents accumulate proximal to obstruction - Intestinal content not absorbed since fluid cannot move along the GI tract - Distention occurs - Peristalsis increases - release of more secretions, further distention -  Edema of bowel, increasing capillary permeability
1. Plasma leaks into the peritoneum - loss of fluids & electrolytes
a. Loss of fluid - hypovolemia
b. Loss of electrolytes - acid-base imbalances


Causes - malabsorption syndrome

1. Bile salt or enzyme deficiency
a. malabsorption of fats & fat-soluble vitamins
b. lactase deficiency

2. Bacteria

3. Disruption of mucosal lining of intestine
a. Celiac disease, Tropical Sprue, Crohn’s disease & Ulcerative colitis

4. Decreased lymphatic or vascular flow

5. Decrease in stomach or intestinal surface area
a. Gastric or intestinal resection - short bowel syndrome 


Lactase deficiency TX

Celiac disease TX 

Lactose-free or restricted diet 


Gluten-free diet -  Gluten is a protein complex found in wheat (including kamut and spelt), barley, rye and triticale


Oral cancer - risk factors 

1) Smoking & chewing tobacco
2) Excessive alcohol use
3) Tanning
4) Strong link with the HPV 


GERD - chronic disorder - contributing factors 

1) Fatty foods, carbonated beverages
2) Chocolate, peppermint, citrus fruits
3) Smoking, alcohol, obesity
4) Medications 


GERD - S/s 

A) Dyspepsia - indigestion or heartburn
B) Regurgitation
C) Excessive gas production resulting in burping, bloating & flatus
D) Resp. symptoms may include cough; increased incidence in pts with asthma


GERD - Nonsurgical & nonpharmacological interventions

Dietary & lifestyle modifications
Avoid acidic, irritating foods
Eat 4-6 small meals a day; remain upright for 1-2 hours after meals
Avoid eating anything for 3 hours before bedtime 


GERD - Drug therapy & SX

Drug therapy
1. Antacids - neutralize acid in the stomach
2. Histamine (H2) blockers - block the H2 receptors on parietal cells
3. Proton Pump Inhibitors (PPI) - inhibiting the hydrogen/potassium ATPase system
4. Prokinetics (Reglan) - facilitate gastric emptying; increase stomach motility

• Laparoscopic Nissen fundoplication  - minimally invasive sx - portion of the stomach fundus is wrapped around the lower esophageal sphincter


GERD - complications 

1) Esophageal scar tissue - leading to strictures
2) Barrett’s esophagus - pre-malignant condition - the lining of the esophagus is damaged by stomach acid and changed to a lining similar to that of the stomach  


Hiatal or diaphragmatic hernias - TX similar to GERD 

A) Sliding hernia - esophagogastric junction and the upper stomach, or fundus, freely
move in & out of the chest through the weakened diaphragm
 Concern - development of GERD and its complications

B) Rolling hernia - esophagogastric junction remains in place, but the fundus of the
stomach and occasionally the greater curvature of the stomach move through the
diaphragm into the chest
 Concerns - volvulus (twisting), obstruction and strangulation


Esophageal cancer - risk factors 

1) Smoking & tobacco use
2) Excessive alcohol intake
3) Long-term, untreated GERD
4) Barrett’s esophagus
5) Achalasia (spasm of LES)
6) Esophageal diverticuli
7) HPV


Esophageal cancer - S/s 

A) Persistent and progressive dysphagia
1) Difficulty swallowing solids, then progressing to increased difficulty swallowing soft foods, then liquids

B) Weight loss

C) Food sticking in throat
D) Increased pain with swallowing
1) Chest pain, regurgitation

E) Cough & increased secretions 


Gastritis - patho

Chronic gastritis 

Protective barrier is lost, a process called autodigestion → inflammation,
edema, bleeding
Chronic gastritis → progressive atrophy of the mucosal lining, interferes with parietal cell function, → decreases production of HCL and intrinsic factor→ Intrinsic factor is
necessary for the absorption of vitamin B12 → Decreased production of intrinsic factor → cobalamin deficiency and pernicious anemia 


Acute gastritis causative factors 

1) Stress
2) H.pylori bacteria - gram-negative bacteria that penetrates the mucosal lining
3) Long-term NSAID use
4) Excessive alcohol & caffeine consumption
5) Certain medications such as corticosteroid
a. NSAIDS inhibit prostaglandin production destroying the stomachs protective barrier 


Gastric ulcer


Duodenal ulcer 


Stress ulcer 

 delayed stomach emptying 


rapid stomach emptying


hospitalized patients
a. NPO status
b. ischemia to mucosal lining


Peptic Ulcer Disease (PUD)

lesion on the gastric or duodenal mucosa 


Prilosec - Omeprazole

Nexium - Esomeprazole 

- prazole meds 

Proton Pump inhibitors 

main tx for more severe GERD 

long-acting inhibition of gastric acid and secretion by affecting the proton pump of the gastric parietal cells 

SE- Hypocalcemia - hip fx

GI infections



Assessment for perforated diverticulum 

Diverticula - food or bacteria trapped - diverticulitis - perforate - local abscess. 

A perforated diverticulum can progress to an intra-abdominal perforation with peritonitis 

Generalized pain


Fever  low grade - chills + tachycardia 

Exam abdomen for profound guarding , rebound tenderness, 

! Sepsis, hypotension, hypovolemic shock 


Itching with gall bladder issues 

Obstructive jaundice - normal flow of bile into duodenum is blocked - allowing excessive bile salts to accumulate in the skin - pruritus or burning sensation 


Cholecystitis: inflammation of the GB
Cholelithiasis – stones in the gallbladder


abnormal metabolism of cholesterol & bile salts
Stones form → irritate the GB wall → inflammation. Stones block cystic duct → trapped bile causes chemical irritation of GB. Irritation → edema & distention → interferes with circulation. Infection & ischemia → necrosis &
gangrene. Severe edema → perforation & peritonitis 


Cholecystitis - TX 

A. Nonsurgical
a. Analgesics – Dilaudid, Morphine
b. Anticholinergics - Bentyl
c. Low fat diet

B. Surgical
a. Laparoscopic Cholecystectomy
i. Carbon dioxide is instilled
ii. Postop shoulder or scapular pain from CO2
b. Choledochoscopy
i. Exploration of common bile duct – remove stones
c. Extracorporeal shockwave lithotripsy (ESWL)
d. Open cholecystectomy
i. Greater risk for complications
ii. Drains
1. Jackson-Pratt (JP)
2. T-Tube